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Abstract

Objectives
To study possible effects of aerosol exposure on lung function, fractional exhaled nitric oxide (FeNO) and inflammatory markers in blood from Norwegian cement production workers across one work shift (0 to 8 h) and again 32 h after the non-exposed baseline registration.

Methods
95 workers from two cement plants in Norway were included. Assessment of lung function included spirometry and gas diffusion pre- and post-shift (0 and 8 h). FeNO concentrations were measured and blood samples collected at 0, 8 and 32 h. Blood analysis included cell counts of leucocytes and mediators of inflammation.

Results
The median respirable aerosol level was 0.3 mg/m3 (range 0.02–6.2 mg/m3). FEV1, FEF25–75% and DLCO decreased by 37 ml (p=0.04), 170 ml/s (p<0.001) and 0.17 mmol/min/kPa (p=0.02), respectively, across the shift. A 2 ppm reduction in FeNO between 0 and 32 h was detected (p=0.01). The number of leucocytes increased by 0.6×109 cells/l (p<0.001) across the shift, while fibrinogen levels increased by 0.02 g/l (p<0.001) from 0 to 32 h. TNF-a level increased and IL-10 decreased across the shift. Baseline levels of fibrinogen were associated with the highest level of respirable dust, and increased by 0.39 g/l (95% CI 0.06 to 0.72).

Conclusions
We observed small cross-shift changes in lung function and inflammatory markers among cement production workers, indicating that inflammatory effects may occur at exposure levels well below 1 mg/m3. However, because the associations between these acute changes and personal exposure measurements were weak and as the long-term consequences are unknown, these findings should be tested in a follow-up study.

Plain text:
Objectives
To study possible effects of aerosol exposure on lung function, fractional exhaled nitric oxide (FeNO) and inflammatory markers in blood from Norwegian cement production workers across one work shift (0 to 8 h) and again 32 h after the non-exposed baseline registration.
Methods
95 workers from two cement plants in Norway were included. Assessment of lung function included spirometry and gas diffusion pre- and post-shift (0 and 8 h). FeNO concentrations were measured and blood samples collected at 0, 8 and 32 h. Blood analysis included cell counts of leucocytes and mediators of inflammation.
Results
The median respirable aerosol level was 0.3 mg/m3 (range 0.02-6.2 mg/m3). FEV1, FEF25-75% and DLCO decreased by 37 ml (p=0.04), 170 ml/s (p<0.001) and 0.17 mmol/min/kPa (p=0.02), respectively, across the shift. A 2 ppm reduction in FeNO between 0 and 32 h was detected (p=0.01). The number of leucocytes increased by 0.6x109 cells/l (p<0.001) across the shift, while fibrinogen levels increased by 0.02 g/l (p<0.001) from 0 to 32 h. TNF-a level increased and IL-10 decreased across the shift. Baseline levels of fibrinogen were associated with the highest level of respirable dust, and increased by 0.39 g/l (95% CI 0.06 to 0.72).
Conclusions
We observed small cross-shift changes in lung function and inflammatory markers among cement production workers, indicating that inflammatory effects may occur at exposure levels well below 1 mg/m3. However, because the associations between these acute changes and personal exposure measurements were weak and as the long-term consequences are unknown, these findings should be tested in a follow-up study.